| First Author | Zechner C | Year | 2010 |
| Journal | Cell Metab | Volume | 12 |
| Issue | 6 | Pages | 633-42 |
| PubMed ID | 21109195 | Mgi Jnum | J:168114 |
| Mgi Id | MGI:4881890 | Doi | 10.1016/j.cmet.2010.11.008 |
| Citation | Zechner C, et al. (2010) Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity. Cell Metab 12(6):633-42 |
| abstractText | Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1alpha(-/-)beta(f/f/MLC-Cre) mice) were generated and characterized. PGC-1alpha(-/-)beta(f/f/MLC-Cre) mice exhibit a dramatic reduction in exercise performance compared to single PGC-1alpha- or PGC-1beta-deficient mice and wild-type controls. The exercise phenotype of the PGC-1alpha(-/-)beta(f/f/MLC-Cre) mice was associated with a marked diminution in muscle oxidative capacity, together with rapid depletion of muscle glycogen stores. In addition, the PGC-1alpha/beta-deficient muscle exhibited mitochondrial structural derangements consistent with fusion/fission and biogenic defects. Surprisingly, the proportion of oxidative muscle fiber types (I, IIa) was not reduced in the PGC-1alpha(-/-)beta(f/f/MLC-Cre) mice. Moreover, insulin sensitivity and glucose tolerance were not altered in the PGC-1alpha(-/-)beta(f/f/MLC-Cre) mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity. |
